ArticleScientific reports2026
HACE1 alleviates intervertebral disc degeneration by inhibiting ferroptosis in nucleus pulposus cells.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
1 citing paper in PubMed.
- A Challenge-Oriented Review of Delivery Systems for Cell and Gene Therapies in Intervertebral Disc Degeneration.Bioengineering (Basel, Switzerland) · 2026Review
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Authors and funding
12 authors.
Funding
Abstract
HACE1 (HECT domain and ankyrin repeat containing E3 ubiquitin protein ligase 1) is an antioxidant gene that plays a key role in activating antioxidant pathways to maintain cellular homeostasis. Recent studies suggest that the antioxidant gene HACE1 may be a potential therapeutic target for age-related degenerative diseases. However, its role in intervertebral disc degeneration (IDD) has not been reported in any study. To clarify the role of HACE1 in IDD, we performed in vivo and in vitro basal experiments. The MRI results indicated that the degeneration grade of intervertebral discs in old rats was significantly higher compared to that in juvenile rats. Additionally, the expression of HACE1 in the degenerated intervertebral discs of aged rats was reduced. In cellular experiments, HACE1 overexpression could restore IL-1β-induced apoptosis, mitochondrial damage and iron overload. In animal experiments, HACE1 activated antioxidant signaling pathways, attenuated oxidative stress, and increased the expression of ECM and anti-ferroptosis proteins. In summary, HACE1 alleviates the progression of IDD by inhibiting oxidative stress and ferroptosis in nucleus pulposus cells. Its protective effect may be related to the activation of the Nrf2/ARE signaling pathway. In conclusion, our results support that the antioxidant gene HACE1 could serve as a novel potential target for treating IDD.
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Registered trials
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